On the Star Class Group of a Pullback

For the domain $R$ arising from the construction $T, M,D$, we relate the star class groups of $R$ to those of $T$ and $D$. More precisely, let $T$ be an integral domain, $M$ a nonzero maximal ideal of $T$, $D$ a proper subring of $k:=T/M$, $\phi: T\to k$ the natural projection, and let $R={\phi}^{-1}(D)$. For each star operation $\ast$ on $R$, we define the star operation $\ast_\phi$ on $D$, i.e., the ``projection'' of $\ast$ under $\phi$, and the star operation ${(\ast)}_{_{T}}$ on $T$, i.e., the ``extension'' of $\ast$ to $T$. Then we show that, under a mild hypothesis on the group of units of $T$, if $\ast$ is a star operation of finite type, 0\to \Cl^{\ast_{\phi}}(D) \to \Cl^\ast(R) \to \Cl^{{(\ast)}_{_{T}}}(T)\to 0 is split exact. In particular, when $\ast = t_{R}$, we deduce that the sequence 0\to \Cl^{t_{D}}(D) {\to} \Cl^{t_{R}}(R) {\to}\Cl^{(t_{R})_{_{T}}}(T) \to 0 is split exact. The relation between ${(t_{R})_{_{T}}}$ and $t_{T}$ (and between \Cl^{(t_{R})_{_{T}}}(T) and \Cl^{t_{T}}(T)) is also investigated.Comment: J. Algebra (to appear

Polynomial extensions of semistar operations

We provide a complete solution to the problem of extending arbitrary semistar operations of an integral domain $D$ to semistar operations of the polynomial ring $D[X]$. As an application, we show that one can reobtain the main results of some previous papers concerning the problem in the special cases of stable semistar operations of finite type or semistar operations defined by families of overrings. Finally, we investigate the behavior of the polynomial extensions of the most important and classical operations such as $d_D$, $v_D$, $t_D$, $w_D$ and $b_D$ operations

Notch1 intracellular domain suppresses APP intracellular domain—Tip60–Fe65 complex mediated signaling through physical interaction

AbstractThe amyloid beta-precursor protein (APP) and the Notch receptor are both type 1 integral transmembrane proteins, and both are cleaved by presenilin-dependent gamma-secretase activity. In this study, we have demonstrated that the Notch intracellular domain (Notch1-IC) suppresses APP-intracellular domain (AICD)-mediated ROS generation and cell death after being processed by gamma secretase. Notch1-IC physically interacts with AICD, Fe65, and Tip60, thereby disrupting the association of the AICD–Fe65–Tip60 trimeric transcription activator complex in AICD signaling. AICD–Fe65–Tip60 mediated reactive oxygen species generation was found to be suppressed by Notch1-IC. Furthermore, AICD–Fe65–Tip60 was shown to mediate cell death in human neuroblastoma cells, and the overexpression of Notch1-IC inhibited cell death induced by AICD–Fe65–Tip60. Collectively, our findings indicate that Notch1-IC plays the role of a negative regulator in AICD signaling via the disruption of the AICD–Fe65–Tip60 trimeric complex

A lab-on-a-disc platform enables serial monitoring of individual CTCs associated with tumor progression during EGFR-targeted therapy for patients with NSCLC

Rationale: Unlike traditional biopsy, liquid biopsy, which is a largely non-invasive diagnostic and monitoring tool, can be performed more frequently to better track tumors and mutations over time and to validate the efficiency of a cancer treatment. Circulating tumor cells (CTCs) are considered promising liquid biopsy biomarkers; however, their use in clinical settings is limited by high costs and a low throughput of standard platforms for CTC enumeration and analysis. In this study, we used a label-free, high-throughput method for CTC isolation directly from whole blood of patients using a standalone, clinical setting-friendly platform. Methods: A CTC-based liquid biopsy approach was used to examine the efficacy of therapy and emergent drug resistance via longitudinal monitoring of CTC counts, DNA mutations, and single-cell-level gene expression in a prospective cohort of 40 patients with epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer. Results: The change ratio of the CTC counts was associated with tumor response, detected by CT scan, while the baseline CTC counts did not show association with progression-free survival or overall survival. We achieved a 100% concordance rate for the detection of EGFR mutation, including emergence of T790M, between tumor tissue and CTCs. More importantly, our data revealed the importance of the analysis of the epithelial/mesenchymal signature of individual pretreatment CTCs to predict drug responsiveness in patients. Conclusion: The fluid-assisted separation technology disc platform enables serial monitoring of CTC counts, DNA mutations, as well as unbiased molecular characterization of individual CTCs associated with tumor progression during targeted therapy

Relationship between Work Hours and Smoking Behaviors in Korean Male Wage Workers

OBJECTIVES: The purposes of this study are 1) to measure the prevalence of smoking according to weekly work hours by using data from the Korean Labor and Income Panel Study (KLIPS), and 2) to explain the cause of high smoking prevalence among those with short or long work hours by relative explanatory fraction. METHODS: Data from a total of 2,044 male subjects who responded to the questionnaire in the 10th year (2007) and 11th year (2008) of the Korean Labor and Income Panel Study were used for analysis. Current smoking, smoking cessation, continuous smoking, start of smoking, weekly work hours, occupational characteristics, sociodemographic and work-related factors, and health behavior-related variables were analyzed. Log-binomial regression analysis was used to study the relationship between weekly work hours and smoking behaviors in terms of the prevalence ratio. RESULTS: The 2008 age-adjusted smoking prevalence was 64.9% in the short work hours group, 54.7% in the reference work hours group, and 60.6% in the long work hours group. The smoking prevalence of the short work hours group was 1.39 times higher than that of the reference work hours group (95% confidence interval of 1.17-1.65), and this was explained by demographic variables and occupational characteristics. The smoking prevalence of the long work hours group was 1.11 times higher than that of the reference work hours group when the age was standardized (95% confidence interval of 1.03-1.19). This was explained by demographic variables. No independent effects of short or long work hours were found when the variables were adjusted. CONCLUSION: Any intervention program to decrease the smoking prevalence in the short work hours group must take into account employment type, job satisfaction, and work-related factors

A simple scoring model for advanced colorectal neoplasm in asymptomatic subjects aged 40–49 years

BACKGROUND: Limited data are available for advanced colorectal neoplasm in asymptomatic individuals aged 40–49 years. We aimed to identify risk factors and develop a simple prediction model for advanced colorectal neoplasm in these persons. METHODS: Clinical data were collected on 2781 asymptomatic subjects aged 40–49 years who underwent colonoscopy for routine health examination. Subjects were randomly allocated to a development or validation set. Logistic regression analysis was used to determine predictors of advanced colorectal neoplasm. RESULTS: The prevalence of overall and advanced colorectal neoplasm was 20.2 and 2.5% respectively. Older age (45–49 years), male sex, positive serology of Helicobacter pylori, and high triglyceride and low high-density lipoprotein (HDL) levels were independently associated with an increased risk of advanced colorectal neoplasm. BMI (body mass index) was not significant in multivariable analysis. We developed a simple scoring model for advanced colorectal neoplasm (range 0–9). A cutoff of ≥4 defined 43% of subjects as high risk for advanced colorectal neoplasm (sensitivity, 79%; specificity, 58%; area under the receiver operating curve = 0.72) in the validation datasets. CONCLUSION: Older age (45–49 years), male sex, positive serology of H. pylori, high triglyceride level, and low HDL level were identified as independent risk factors for advanced colorectal neoplasm

Visfatin exerts angiogenic effects on human umbilical vein endothelial cells through the mTOR signaling pathway

AbstractThe biologically active factors known as adipocytokines are secreted primarily by adipose tissues and can act as modulators of angiogenesis. Visfatin, an adipocytokine that has recently been reported to have angiogenic properties, is upregulated in diabetes, cancer, and inflammatory diseases. Because maintenance of an angiogenic balance is critically important in the management of these diseases, understanding the molecular mechanism by which visfatin promotes angiogenesis is very important. In this report, we describe our findings demonstrating that visfatin stimulates the mammalian target of the rapamycin (mTOR) pathway, which plays important roles in angiogenesis. Visfatin induced the expression of hypoxia-inducible factor 1α (HIF1α) and vascular endothelial growth factor (VEGF) in human endothelial cells. Inhibition of the mTOR pathway by rapamycin eliminated the angiogenic and proliferative effects of visfatin. The visfatin-induced increase in VEGF expression was also eliminated by RNA interference-mediated knockdown of the 70-kDa ribosomal protein S6 kinase (p70S6K), a downstream target of mTOR. Visfatin inactivated glycogen synthase kinase 3β (GSK3β) by phosphorylating it at Ser-9, leading to the nuclear translocation of β-catenin. Both rapamycin co-treatment and p70S6K knockdown inhibited visfatin-induced GSK3β phosphorylation at Ser-9 and nuclear translocation of β-catenin. Taken together, these results indicate that mTOR signaling is involved in visfatin-induced angiogenesis, and that this signaling leads to visfatin-induced VEGF expression and nuclear translocation of β-catenin